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Fibromyalgia: Difference between revisions

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{{Curriculum}}{{stub}}{{Controversial}}
{{Curriculum}}{{stub}}{{Controversial}}
Fibromyalgia is a chronic medical condition that is characterised by widespread pain, fatigue, waking unrefreshed and cognitive disorders. It is the prototypical centralised pain state. In the field of musculoskeletal medicine in New Zealand, the highly subjective nature of the diagnostic criteria has meant that it is a controversial diagnosis in this specialty. Recent work has found that 40-50% of patients have [[Small Fibre Neuropathy|small fibre neuropathy]].<ref name="Maslinska">Maslinska et al. Small fibre neuropathy as a part of fibromyalgia or a separate diagnosis? Int. J. Clin. Rheumatol. (2018) 13(6), 353-359. [https://www.openaccessjournals.com/articles/small-fiber-neuropathy-as-a-part-of-fibromyalgia-or-a-separate-diagnosis.pdf Full Text]</ref>
Fibromyalgia is a lifelong medical condition that is characterised by widespread pain, fatigue, waking unrefreshed and cognitive disorders. It is the prototypical [[Nociplastic Pain|centralised pain state]] where there is a fundamental problem with augmented pain or sensory processing and manifests in different parts of the body over time. While mental health complaints are common, the pain itself is not psychosomatic in nature.


==Epidemiology==
==Epidemiology==
Fibromyalgia is present across the world, and has a prevalence ranging between 2% to 4%. 10-15% of the population have chronic widespread pain, and there is no clear boundary separating those that have chronic widespread pain from those that have fibromyalgia. The peak onset is 20-50. and is more common in women. In clinical practice it is predominantly diagnosed in women in late middle age. Other risk factors are increasing age, family history of chronic pain, obesity, and poor mental and/or physical health.
Fibromyalgia is present across the world, and has a prevalence ranging between 2% to 4%. It is the second most common rheumatological disorder after osteoarthritis. 10-15% of the population have chronic widespread pain, and there is no clear boundary separating those that have chronic widespread pain from those that have fibromyalgia. Ā 
Ā 
The peak onset is 20-50 but it can occur at any age. and is about twice as common in women. In clinical practice it is predominantly diagnosed in women in late middle age. Other risk factors are increasing age, family history of chronic pain, obesity, and poor mental and/or physical health. It occurs in all countries and ethnicities.


Patients with fibromyalgia have roughly double the healthcare utilization compared to matched controls for at least a decade prior to diagnosis. Visits increase rapidly three years prior to diagnosis, then slightly decline after diagnosis, and rise again three years post-diagnosis, remaining at levels comparable to diagnosis but never reaching the level of two years prior to diagnosis. The overall benefit of the diagnostic process and medical input appears questionable at the population level.<ref name=":2">{{Cite journal|last=Hughes|first=Gwenda|last2=Martinez|first2=Carlos|last3=Myon|first3=Eric|last4=TaĆÆeb|first4=Charles|last5=Wessely|first5=Simon|date=2006-01|title=The impact of a diagnosis of fibromyalgia on health care resource use by primary care patients in the UK: an observational study based on clinical practice|url=https://pubmed.ncbi.nlm.nih.gov/16385513|journal=Arthritis and Rheumatism|volume=54|issue=1|pages=177ā€“183|doi=10.1002/art.21545|issn=0004-3591|pmid=16385513}}</ref>
Patients with fibromyalgia have roughly double the healthcare utilization compared to matched controls for at least a decade prior to diagnosis. Visits increase rapidly three years prior to diagnosis, then slightly decline after diagnosis, and rise again three years post-diagnosis, remaining at levels comparable to diagnosis but never reaching the level of two years prior to diagnosis. The overall benefit of the diagnostic process and medical input appears questionable at the population level.<ref name=":2">{{Cite journal|last=Hughes|first=Gwenda|last2=Martinez|first2=Carlos|last3=Myon|first3=Eric|last4=TaĆÆeb|first4=Charles|last5=Wessely|first5=Simon|date=2006-01|title=The impact of a diagnosis of fibromyalgia on health care resource use by primary care patients in the UK: an observational study based on clinical practice|url=https://pubmed.ncbi.nlm.nih.gov/16385513|journal=Arthritis and Rheumatism|volume=54|issue=1|pages=177ā€“183|doi=10.1002/art.21545|issn=0004-3591|pmid=16385513}}</ref>


The most common reasons for clinical visits in order of frequency are depression, fatigue, chest pain, headache, sleep disturbance, dizziness, and IBS.<ref name=":2" />
Nearly all patients that are eventually diagnosed with fibromyalgia have a long history of having bouts of chronic regional pain various body regions over their lifetime dating back to adolescence.<ref name=":0" /> The most common reasons for clinical visits to GPs in order of frequency are depression, fatigue, chest pain, headache, sleep disturbance, dizziness, and IBS.<ref name=":2" />
Ā 
==Risk Factors==
There is often a strong familial predisposition to pain. Twin studies show that the risk of developing fibromyalgia is 50% genetic and 50% environmental. First degree relatives are more than 8 times as likely to also have fibromyalgia compared to controls. Many of the genes discovered thus far are involved in the regulation of neurotransmitters that modulate pain sensitivity, but genetic studies are not universally consistent and pain sensitivity is polygenic.<ref name=":0" />
Ā 
Psychological and other stressors are often a factor in the development and maintenance of the disorder, with the presence of sympathetic dysfunction,{{#pmid:30238382|manuel}} however it is not a psychosomatic condition. Environmental stressors are often identified, particularly those where there is acute pain that lasts a few weeks. For example motor vehicle accidents or certain infections.


== History ==
Fibromyalgia is frequently observed as a comorbidity in other chronic pain conditions such as OA, RA, and lupus. About 15-30% of individuals with these rheumatic disorders meet FM criteria, and more individuals do not meet the criteria but display some FM elements, indicating the presence of pathophysiological abnormalities in CNS pain processing. The term "centralized pain" rather than "central sensitisation" is preferred when CNS factors play a significant role in magnifying pain and leading to other somatic symptoms.<ref name=":0" />
See review by Hauser and colleagues.<ref name=":1">{{Cite journal|last=HƤuser|first=Winfried|last2=Sarzi-Puttini|first2=Piercarlo|last3=Fitzcharles|first3=Mary-Ann|date=2019|title=Fibromyalgia syndrome: under-, over- and misdiagnosis|url=https://pubmed.ncbi.nlm.nih.gov/30747096|journal=Clinical and Experimental Rheumatology|volume=37 Suppl 116|issue=1|pages=90ā€“97|issn=0392-856X|pmid=30747096}}</ref>


==Pathophysiology==
== Pathophysiology ==
A popular hypothesis is that fibromyalgia is a [[Central Sensitisation|centralised pain syndrome]]. This hypothesis describes fibromyalgia patients as having augmented pain, and augmented sensory processing in the brain. There is increased connectivity to pro-nociceptive brain regions, and decreased connectivity to anti-nociceptive regions. Psychological and other stressors are often a factor in the development and maintenance of the disorder, with the presence of sympathetic dysfunction.{{#pmid:30238382|manuel}}
The current accepted hypothesis is that fibromyalgia is a [[Central Sensitisation|centralised pain syndrome]]. This hypothesis describes fibromyalgia patients as having augmented pain, and augmented sensory processing in the brain. There is increased connectivity to pro-nociceptive brain regions, and decreased connectivity to anti-nociceptive regions. Ā 


Fibromyalgia has also been described as a sympathetically maintained or dysautonomia-relatedĀ  neuropathic pain syndrome. The pain has neuropathic features, and is independent of stimulus, and may be accompanied by allodynia and paraesthesias. Nociceptive fibres may be sensitised.<ref name="manuel" />
Fibromyalgia has also been described as a sympathetically maintained or dysautonomia-relatedĀ  neuropathic pain syndrome. The pain has neuropathic features, and is independent of stimulus, and may be accompanied by allodynia and paraesthesias. Nociceptive fibres may be sensitised.<ref name="manuel" />
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==Differential Diagnosis ==
==Differential Diagnosis ==
The differential diagnosis must be viewed from two different perspectives. The first perspective is recognising that fibromyalgia type symptoms can occur as a co-morbidity alongside another condition. Fibromyalgia occurs alongside 15-30% of individuals with any autoimmune or chronic musculoskeletal pain condition when there is ongoing nociceptive input. This includes [[Rheumatoid Arthritis]] (12-20%), [[Spondyloarthritis]] (11-50%), lupus erythematosus (5-25%)<ref name=":1" />, [[Ehlers Danlos Syndrome|Ehlers-Danlos syndrome]], sickle cell disease, and cancer pain.
The differential diagnosis must be viewed from two different perspectives. The first perspective is recognising that fibromyalgia type symptoms can occur as a co-morbidity alongside another condition. Fibromyalgia occurs alongside 15-30% of individuals with any autoimmune or chronic musculoskeletal pain condition when there is ongoing nociceptive input. This includes [[Rheumatoid Arthritis]] (12-20%), [[Spondyloarthritis]] (11-50%), lupus erythematosus (5-25%)<ref name=":1">{{Cite journal|last=HƤuser|first=Winfried|last2=Sarzi-Puttini|first2=Piercarlo|last3=Fitzcharles|first3=Mary-Ann|date=2019|title=Fibromyalgia syndrome: under-, over- and misdiagnosis|url=https://pubmed.ncbi.nlm.nih.gov/30747096|journal=Clinical and Experimental Rheumatology|volume=37 Suppl 116|issue=1|pages=90ā€“97|issn=0392-856X|pmid=30747096}}</ref>, [[Ehlers Danlos Syndrome|Ehlers-Danlos syndrome]], sickle cell disease, and cancer pain.


The second perspective is understanding that some conditions can mimic the symptoms and so the patient has a different diagnosis entirely, and fibromyalgia is not a comorbidity. Examples of this are [[Polymyalgia Rheumatica and Giant Cell Arteritis|Polymyalgia Rheumatica]], hypothyroidism, and some neuromuscular conditions like statin-induced myopathy.<ref name=":0">Hochberg. Fibryomyalgia In: Rheumatology. 2019</ref>
The second perspective is understanding that some conditions can mimic the symptoms and so the patient has a different diagnosis entirely, and fibromyalgia is not a comorbidity. Examples of this are [[Polymyalgia Rheumatica and Giant Cell Arteritis|Polymyalgia Rheumatica]], hypothyroidism, and some neuromuscular conditions like statin-induced myopathy.<ref name=":0">Hochberg. Fibryomyalgia In: Rheumatology. 2019</ref>
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*[[Small Fibre Neuropathy]]
*[[Small Fibre Neuropathy]]
*[[Central Sensitisation]]
*[[Central Sensitisation]]
== History of the condition ==
See review by Hauser and colleagues.<ref name=":1" />


==References==
==References==

Revision as of 21:58, 22 February 2023

This article is a stub.
This page or section deals with a controversial topic.
Please use your clinical judgement.

Fibromyalgia is a lifelong medical condition that is characterised by widespread pain, fatigue, waking unrefreshed and cognitive disorders. It is the prototypical centralised pain state where there is a fundamental problem with augmented pain or sensory processing and manifests in different parts of the body over time. While mental health complaints are common, the pain itself is not psychosomatic in nature.

Epidemiology

Fibromyalgia is present across the world, and has a prevalence ranging between 2% to 4%. It is the second most common rheumatological disorder after osteoarthritis. 10-15% of the population have chronic widespread pain, and there is no clear boundary separating those that have chronic widespread pain from those that have fibromyalgia.

The peak onset is 20-50 but it can occur at any age. and is about twice as common in women. In clinical practice it is predominantly diagnosed in women in late middle age. Other risk factors are increasing age, family history of chronic pain, obesity, and poor mental and/or physical health. It occurs in all countries and ethnicities.

Patients with fibromyalgia have roughly double the healthcare utilization compared to matched controls for at least a decade prior to diagnosis. Visits increase rapidly three years prior to diagnosis, then slightly decline after diagnosis, and rise again three years post-diagnosis, remaining at levels comparable to diagnosis but never reaching the level of two years prior to diagnosis. The overall benefit of the diagnostic process and medical input appears questionable at the population level.[1]

Nearly all patients that are eventually diagnosed with fibromyalgia have a long history of having bouts of chronic regional pain various body regions over their lifetime dating back to adolescence.[2] The most common reasons for clinical visits to GPs in order of frequency are depression, fatigue, chest pain, headache, sleep disturbance, dizziness, and IBS.[1]

Risk Factors

There is often a strong familial predisposition to pain. Twin studies show that the risk of developing fibromyalgia is 50% genetic and 50% environmental. First degree relatives are more than 8 times as likely to also have fibromyalgia compared to controls. Many of the genes discovered thus far are involved in the regulation of neurotransmitters that modulate pain sensitivity, but genetic studies are not universally consistent and pain sensitivity is polygenic.[2]

Psychological and other stressors are often a factor in the development and maintenance of the disorder, with the presence of sympathetic dysfunction,[3] however it is not a psychosomatic condition. Environmental stressors are often identified, particularly those where there is acute pain that lasts a few weeks. For example motor vehicle accidents or certain infections.

Fibromyalgia is frequently observed as a comorbidity in other chronic pain conditions such as OA, RA, and lupus. About 15-30% of individuals with these rheumatic disorders meet FM criteria, and more individuals do not meet the criteria but display some FM elements, indicating the presence of pathophysiological abnormalities in CNS pain processing. The term "centralized pain" rather than "central sensitisation" is preferred when CNS factors play a significant role in magnifying pain and leading to other somatic symptoms.[2]

Pathophysiology

The current accepted hypothesis is that fibromyalgia is a centralised pain syndrome. This hypothesis describes fibromyalgia patients as having augmented pain, and augmented sensory processing in the brain. There is increased connectivity to pro-nociceptive brain regions, and decreased connectivity to anti-nociceptive regions.

Fibromyalgia has also been described as a sympathetically maintained or dysautonomia-related neuropathic pain syndrome. The pain has neuropathic features, and is independent of stimulus, and may be accompanied by allodynia and paraesthesias. Nociceptive fibres may be sensitised.[3]

Clinical Features

The patient may report persistent pain for over three months, pain in more than one region, intrusive fatigue, impaired memory ("fibro fog"), sleep disturbance, and gastrointestinal disturbance. Other symptoms include increased pain sensitivity (e.g. pain with hugging), muscle stiffness, headaches, anxiety, depression, and irregular periods.

A complete rheumatological, orthopaedic, and neurological examination should be performed.

Diagnosis

Fibromyalgia is over diagnosed. In one study in the US, the majority of individuals with a clinical diagnosis of fibromyalgia do not fulfil the diagnostic criteria.[4]

2010 Criteria

Fibromyalgia Diagnostic Criteria 2010.pdf

In 2010 the American College of Rheumatology (ACR) revamped the diagnostic criteria. There is no requirement for a tender point examination like in the ACR 1990 classification. Three criteria must be met for the diagnosis

  1. Widespread Pain Index (WPI) ā‰„ 7/19 and Symptom Severity Scale (SSS) Score ā‰„ 5/12 or WPI between 3ā€“6/19 and SSS ā‰„ 9/12
  2. Symptoms being present at a similar level for at least 3 months
  3. The patient does not have another disorder that would otherwise sufficiently explain the pain.

Conditions 1 and 2 are assessed by the Fibromyalgia Survey Questionnaire.

2016 Criteria

Fibromyalgia diagnostic criteria 2016.pdf

The criteria were modified in 2016. A major change was that other conditions don't need to be ruled out and it can be diagnosed irrespective of other diagnoses.

Differential Diagnosis

The differential diagnosis must be viewed from two different perspectives. The first perspective is recognising that fibromyalgia type symptoms can occur as a co-morbidity alongside another condition. Fibromyalgia occurs alongside 15-30% of individuals with any autoimmune or chronic musculoskeletal pain condition when there is ongoing nociceptive input. This includes Rheumatoid Arthritis (12-20%), Spondyloarthritis (11-50%), lupus erythematosus (5-25%)[5], Ehlers-Danlos syndrome, sickle cell disease, and cancer pain.

The second perspective is understanding that some conditions can mimic the symptoms and so the patient has a different diagnosis entirely, and fibromyalgia is not a comorbidity. Examples of this are Polymyalgia Rheumatica, hypothyroidism, and some neuromuscular conditions like statin-induced myopathy.[2]

A problem occurs when considering another disease that has clinical features that can be similar to those with fibromyalgia. An obvious example is metastatic cancer.

Differential Diagnosis of Widespread Pain

Small Fibre Neuropathy

Main article: Small Fibre Neuropathy

There has been a large amount of research confirming the presence of small fibre neuropathy (SFN) in some fibromyalgia patients. Overall it appears that around 40-50% of fibromyalgia patients actually have SFN - a neuropathic pain syndrome.

For example, Oaklander et al found that in 41 patients with unexplained widespread pain that started before the age of 21, 59% of children at definite SFN, 17% had probable SFN, and 22% had possible SFN.[6] They then found that in a group of 27 fibromyalgia patients and 30 matched controls, 41% of fibromyalgia patients had definite SFN, compared to 3% in the control group.[7] See Manuel et al for a summary.[3]

Some central sensitisation framework proponents claim that the presence of small fibre neuropathy has unclear relevance, and may be a consequence not a cause of fibromyalgia, with peripheral nervous system changes in response to central nervous system sensitisation. This view is not universally shared. Manuel et al believe fibromyalgia to be related to a persistent hyper-adrenergic state, leading to dorsal root ganglia hyper-excitability, and neuropathic pain. They note the role of dorsal root ganglia sodium channel variants in the condition.[3]

Investigations

First line screening tests to exclude somatic disease are FBC, CRP, CK, calcium, TSH.

Other tests to consider are ESR, LFTs, glucose, UEC.

Vitamin D levels are low in the majority of patients with chronic pain, but this test is not funded in NZ.[2]

If there is suspicion of axial spondyloarthritis then consider HLA-B27, and RF if psoriatic.

If there is suspicion of Rheumatoid Arthritis then include anti-CCP, and RF.

ANA can be considered if there are consistent clinical features.

Treatment

There is no highly effective treatment. Exercise is first line, medication is second line.

Resources

Fibromyalgia Diagnostic Criteria 2016 Article - Wolfe 2016.pdf

See Also

History of the condition

See review by Hauser and colleagues.[5]

References

  1. ā†‘ 1.0 1.1 Hughes, Gwenda; Martinez, Carlos; Myon, Eric; TaĆÆeb, Charles; Wessely, Simon (2006-01). "The impact of a diagnosis of fibromyalgia on health care resource use by primary care patients in the UK: an observational study based on clinical practice". Arthritis and Rheumatism. 54 (1): 177ā€“183. doi:10.1002/art.21545. ISSN 0004-3591. PMID 16385513. Check date values in: |date= (help)
  2. ā†‘ 2.0 2.1 2.2 2.3 2.4 Hochberg. Fibryomyalgia In: Rheumatology. 2019
  3. ā†‘ 3.0 3.1 3.2 3.3 MartĆ­nez-LavĆ­n. Fibromyalgia and small fiber neuropathy: the plot thickens!. Clinical rheumatology 2018. 37:3167-3171. PMID: 30238382. DOI.
  4. ā†‘ Walitt B, Katz RS, Bergman MJ, Wolfe F. Three-Quarters of Persons in the US Population Reporting a Clinical Diagnosis of Fibromyalgia Do Not Satisfy Fibromyalgia Criteria: The 2012 National Health Interview Survey. PLoS One. 2016 Jun 9;11(6):e0157235. doi: 10.1371/journal.pone.0157235. PMID: 27281286; PMCID: PMC4900652.
  5. ā†‘ 5.0 5.1 HƤuser, Winfried; Sarzi-Puttini, Piercarlo; Fitzcharles, Mary-Ann (2019). "Fibromyalgia syndrome: under-, over- and misdiagnosis". Clinical and Experimental Rheumatology. 37 Suppl 116 (1): 90ā€“97. ISSN 0392-856X. PMID 30747096.
  6. ā†‘ Oaklander & Klein. Evidence of small-fiber polyneuropathy in unexplained, juvenile-onset, widespread pain syndromes. Pediatrics 2013. 131:e1091-100. PMID: 23478869. DOI. Full Text.
  7. ā†‘ Oaklander et al.. Objective evidence that small-fiber polyneuropathy underlies some illnesses currently labeled as fibromyalgia. Pain 2013. 154:2310-6. PMID: 23748113. DOI. Full Text.

Literature Review

Library.pngLiterature Review

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